My overall objective is to discover why the lens of the rat fed a diet deficient in the amino acid, tryptophan, ceases to grow at the normal rate and becomes cataractous. In preliminary experiments I have observed a consistent pattern of lens changes in rats, which remain alive and healthy on a tryptophan-deficient diet (0.087% tryptophan). In the past (when a diet almost devoid of tryptophan was used) a high mortality rate prevented study of this type of cataract. Litters of weanling rats will be divided into two groups, one fed the deficient diet, and the other with 0.2% L-tryptophan added. The eyes will be examined regularly and the animals killed at intervals. Blood and eye tissues will be analysed for tryptophan and the lenses for the following: wet and dry weight, water- and urea-soluble protein, Na ion, and other ions, glutathione, ribonuclease, free amino acids, etc. The possible reversibility of the cataract will be studied, and whether other agents (e.g. X-rays, galactose) exert a synergistic effect. Detailed biochemical investigations will fall under three main headings, (1) What changes occur in the proteins of the lens? (2) Is decreased growth due to decreased protein synthesis, increased proteolysis or both? (3) What is the effect on the maturation of lens fibres? Preliminary experiments have shown that the epithelial cells do not mature normally into fibres. The ultimate goal is to discover more about the causes of senile cataract in man. This may be the largest single cause of blindness; about 1.25 million people are affected yearly. There are probably many different causes, superimposed upon the normal aging process. Dietary insufficiency has frequently been mooted but not proved. Tryptophan deficiency in rats is a promising model system in which to study changes leading to cataract. Any changes observed would give a clue to changes to look for in the senile cataractous lens of man, normal post-mortem lenses being used as controls.